Human immunodeficiency virus (HIV) is subdivided into 2 types, HIV-1 and HIV-2, both of which are believed to be the result of separate zoonotic transmissions on at least eight different occasions (Hahn et al., Science 287:607-17, 2000; Sharp et al., Philos Trans R Soc Lond B Biol Sci 356:867-6, 2001) from chimpanzees and sooty mangabeys, respectively (Huet et al., Nature 345:356-359, 1990; Gao et al., Nature 397:436-441, 1999; Hirsch et al., Nature 339:389-392, 1989). While the origin of HIV-1 from chimpanzees is mainly supported by the phylogenetic clustering of HIV-1 and SIVcpz, substantial evidence supports the zoonotic origin of HIV-2, including similarity in the viral genome organization, phylogenetic relatedness, prevalence in the natural host, geographic coincidence and plausible route of transmission (Sharp et al., Philos Trans R Soc Lond B Biol Sci 349:41-47, 1995).
There is no evidence that the other lineages of simian immunodeficiency virus (SIV) have crossed into humans. The other lineages include: the SIVagm from four species of African green monkeys; the SIVsyk from sykes' monkeys; the SIVmnd from a mandrill together with SIVlhoest from l'Hoest monkeys and SIVsun from Sun-tailed monkeys; and the SIVcol from a colobus monkey. SIVs from other non-human primates from Africa have been partially sequenced and may represent new lineages. Continued study of SIV is critical for elucidating the origin and spread of HIV in humans, and monitoring future viral threats to humans.
A number of studies have provided serological evidence (using commercially available HIV tests) of SIV infections in at least 30 African non-human primates to date with viral molecular evidence in 24 of the infections (Hahn et al., Science 287:607-617, 2000; Lowenstine et al., Int J Cancer 38:563-574, 1986; Nicol et al., J Med Primatol 18:227-236, 1989; Peeters et al, Emerg Infect Dis 8:451-457, 2002). Humans are also now being increasingly exposed to the many different SIVs in different species of wild primates, for example through the hunting and butchering trade in Sub-Saharan Africa, particularly in Cameroon. This increasing human exposure to the plethora of SIVs prevalent in different species of wild primates may lead, or has already led, to additional transmissions of SIVs with the potential to cause new epidemics. Unfortunately, new zoonotic transmissions may easily go undetected because of the lack of SIV-specific tests.
There is no commercially available test specifically designed for detecting all known SIVs. Serological detection of SIVs has so far been done using HIV tests (Tsujimoto et al., Nature 341:539-541, 1989; Peeters et al., AIDS 6:447-451, 1992; Peeters et al, AIDS Res Hum Retroviruses 10:1289-1294, 1994; Georges-Courbot et al., J Virol 72:600-608, 1998; Beer et al, J Virol 73:7734-7744, 1999; Hirsch et al., Virol 73:1036-1045, 1999; Osterhaus et al, Virology 260:116-124, 1999) based on some cross reactivities observed with SIV antibodies to some HIV antigens. It has not been established whether all SIV strains could be detected in this way and as such, some can readily be missed (Simon et al., AIDS Res Hum Retroviruses 17:937-952, 2001; Peeters et al., Emerg Infect Dis 8:451-457, 2002) due to the high genetic diversity among primate lentiviruses. Indeed, some seronegative monkeys have been found to be infected only as determined by PCR and sequencing (Peeters et al., Emerg Infect Dis 8:451-457, 2002). It would therefore be useful to develop and implement testing methods and strategies sensitive and specific enough to detect diverse SIV strains in monkeys and humans in the event of zoonotic jumps to identify primary infection and prevent secondary transmission that could lead to yet another HIV-like epidemic.